Enterococcus faecalis is a species of bacteria existing as both a normal inhabitant of the body and a formidable disease-causing agent. This microorganism is a Gram-positive bacterium, meaning it possesses a thick layer of peptidoglycan in its cell wall that retains a specific stain used for identification. Its ability to survive in harsh environments and its increasing role as a pathogen in clinical settings make it important. The dual nature of E. faecalis means it rarely causes trouble in healthy individuals but can launch severe, difficult-to-treat infections when given the opportunity.
Enterococcus faecalis as a Commensal Organism
This bacterium is a common resident of the human gastrointestinal tract, where it thrives alongside other microbes. It is a facultative anaerobe, allowing it to adapt and grow across a range of oxygen conditions, from the oxygen-poor large intestine to other mucosal sites. While most prevalent in the gut, E. faecalis is also frequently isolated from the genitourinary tract and the oral cavity in healthy people.
In its role as a commensal organism, E. faecalis contributes to the stability of the gut environment. It participates in the metabolism of various nutrients and helps maintain a balanced intestinal pH. Furthermore, its presence helps prevent the establishment of more harmful bacterial species through colonization resistance. By occupying space and competing for resources, the resident population limits the ability of external pathogens to proliferate.
Mechanisms Driving Pathogenicity
The transition of E. faecalis from a harmless commensal to an opportunistic pathogen typically requires a disruption of the body’s natural defenses or a breach of mucosal barriers. Such conditions often occur in hospital environments, affecting patients with weakened immune systems, those undergoing surgery, or individuals with indwelling medical devices. Once outside its normal habitat, the bacterium employs virulence factors to establish infection.
A primary tool is its ability to adhere tightly to host tissues and surfaces using specialized surface proteins, such as the aggregation substance and Adhesin to Collagen of E. faecalis (Ace). This adhesion is a precursor to forming a biofilm, a protective matrix that encases the bacterial community. Biofilms are problematic on medical equipment like catheters or heart valves, allowing the bacteria to persist, evade the immune response, and resist antibiotic penetration.
E. faecalis also produces enzymes and toxins that contribute to tissue damage and spread. One factor is cytolysin, a secreted toxin that breaks down various host cells, which is associated with severe outcomes in bloodstream infections. Another enzyme is gelatinase (GelE), a metalloprotease that degrades proteins like collagen and hemoglobin, effectively breaking down host tissues to facilitate bacterial invasion.
Common Infections Caused by E. faecalis
When these virulence mechanisms are activated, E. faecalis is responsible for healthcare-associated infections (HAIs). Urinary Tract Infections (UTIs) are the most common form, frequently linked to the use of urinary catheters which provide a surface for biofilm formation and a pathway for the bacteria to ascend the tract. The bacterium can also cause serious wound and soft tissue infections, especially following abdominal or pelvic surgery.
A serious threat occurs when the bacteria enter the bloodstream, resulting in bacteremia. If left unchecked, this can lead to the seeding of distant sites in the body, with endocarditis being a severe complication. Endocarditis is an infection of the inner lining of the heart and its valves, where E. faecalis can establish a persistent, difficult-to-treat biofilm. E. faecalis is a frequent cause of enterococcal endocarditis, a condition that often requires prolonged, aggressive treatment.
The Crisis of Drug-Resistant Enterococci
The challenge of treating E. faecalis infections stems from its intrinsic resistance to many common antibiotics. This species possesses a built-in ability to withstand the effects of certain drug classes, including most cephalosporins and some beta-lactams, making the selection of an effective initial therapy difficult.
The most pressing public health concern involves acquired resistance to vancomycin. Strains that have developed resistance to this drug are known as Vancomycin-Resistant Enterococci (VRE). VRE strains, which include E. faecalis, acquire resistance by obtaining specific genes, such as vanA or vanB, usually carried on mobile genetic elements like plasmids.
These genes allow the bacteria to chemically alter the cell wall structure, changing the target site so that vancomycin can no longer bind effectively and disrupt cell wall synthesis. The rise of VRE is problematic in hospital settings, where the heavy use of antibiotics creates selective pressure for resistant organisms to flourish and spread. This resistance limits treatment options for severe infections like VRE bacteremia, which is associated with increased mortality and longer hospital stays. Containing the spread of VRE relies heavily on stringent infection control practices, including rigorous hand hygiene and environmental cleaning, to break the chain of transmission.